A variety of diseases including asthma, cancers, heart diseases, autoimmune diseases, and viral infections manifest varying symptoms and signs and yet it has been suggested that either an overexpression or underexpression of one or a few proteins is a major etiologic factor in many cases. Moreover, a variety of transcriptional regulatory factors such as transcription activators and transcription inhibitors are involved in the expression of proteins. NF-.kappa.B, a substance known to be one of such transcriptional regulatory factors, is a heterodimer of p65 and p50 proteins. In the cytoplasm, NF-.kappa.B is usually present as substance binding with I.kappa.B, an inhibition factor, and thereby prevented from migrating into the nucleus. However, when a cell is stimulated by cytokines, ischemia, or reperfusion for whatever reason, I.kappa.B is phosphorylated and decomposed so that the NF-.kappa.B is activated and penetrates into the nucleus. NF-.kappa.B attaches itself to the NF-.kappa.B binding site of the chromosome and then promotes transcription of the gene located at downstreams. The gene controlled by NF-.kappa.B includes cytokines such as IL-1, IL-6, IL-8, etc. and adhesion factors such as VCAM-1, ICAM-1, etc . . .